Mouse Monoclonal AKR1C2 antibody. Suitable for WB, ICC/IF and reacts with Mouse, Rat, Human samples. Cited in 4 publications.
pH: 7.5
Preservative: 0.02% Sodium azide
Constituents: 0.877% Sodium chloride, 0.357% HEPES
WB | ICC/IF | |
---|---|---|
Human | Tested | Tested |
Mouse | Tested | Expected |
Rat | Tested | Expected |
Cow | Predicted | Predicted |
Rabbit | Predicted | Predicted |
Species | Dilution info | Notes |
---|---|---|
Species Mouse | Dilution info 2 µg/mL | Notes - |
Species Rat | Dilution info 2 µg/mL | Notes - |
Species Human | Dilution info 2 µg/mL | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Rabbit, Cow | Dilution info - | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Human | Dilution info 5 µg/mL | Notes (paraformaldehyde fixed cells) |
Species | Dilution info | Notes |
---|---|---|
Species Mouse, Rat | Dilution info Use at an assay dependent concentration. | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Rabbit, Cow | Dilution info - | Notes - |
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Cytosolic aldo-keto reductase that catalyzes the NADH and NADPH-dependent reduction of ketosteroids to hydroxysteroids (PubMed:19218247). Most probably acts as a reductase in vivo since the oxidase activity measured in vitro is inhibited by physiological concentrations of NADPH (PubMed:14672942). Displays a broad positional specificity acting on positions 3, 17 and 20 of steroids and regulates the metabolism of hormones like estrogens and androgens (PubMed:10998348). Works in concert with the 5-alpha/5-beta-steroid reductases to convert steroid hormones into the 3-alpha/5-alpha and 3-alpha/5-beta-tetrahydrosteroids. Catalyzes the inactivation of the most potent androgen 5-alpha-dihydrotestosterone (5-alpha-DHT) to 5-alpha-androstane-3-alpha,17-beta-diol (3-alpha-diol) (PubMed:15929998, PubMed:17034817, PubMed:17442338, PubMed:8573067). Also specifically able to produce 17beta-hydroxy-5alpha-androstan-3-one/5alphaDHT (PubMed:10998348). May also reduce conjugated steroids such as 5alpha-dihydrotestosterone sulfate (PubMed:19218247). Displays affinity for bile acids (PubMed:8486699).
DDH2, AKR1C2, Aldo-keto reductase family 1 member C2, 3-alpha-HSD3, Chlordecone reductase homolog HAKRD, Dihydrodiol dehydrogenase 2, Dihydrodiol dehydrogenase/bile acid-binding protein, Type III 3-alpha-hydroxysteroid dehydrogenase, DD-2, DD2, DD/BABP
Mouse Monoclonal AKR1C2 antibody. Suitable for WB, ICC/IF and reacts with Mouse, Rat, Human samples. Cited in 4 publications.
pH: 7.5
Preservative: 0.02% Sodium azide
Constituents: 0.877% Sodium chloride, 0.357% HEPES
Purity >90% by SDS-PAGE.
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The AKR1C1 and AKR1C2 are members of the aldo-keto reductase family. These enzymes also known as dihydrodiol dehydrogenases reduce a variety of substrates including steroids prostaglandins and xenobiotics. AKR1C1 has a molecular mass of approximately 37 kDa while AKR1C2 has a similar but slightly distinct mass. These proteins are expressed in various tissues including the liver prostate and mammary glands where they perform their enzymatic functions.
The AKR1C1/AKR1C2 enzymes play significant roles in steroid hormone metabolism. They modulate the conversion of active hormones to their inactive forms and vice versa affecting the cellular concentration of these hormones. The proteins do not function as part of a larger complex but influence multiple biochemical processes through their enzymatic actions. Their roles in the regulation of sex steroids are important for maintaining normal cellular activity and tissue homeostasis.
AKR1C1 and AKR1C2 are involved in intricate steroid hormone signaling and metabolism pathways. They engage with the androgen and estrogen receptor signaling pathways by modulating hormone availability. The interplay with enzymes like 5-alpha reductase and aromatase highlights their role in the balance of active and inactive hormone forms within these pathways. Their function can influence cellular proliferation and differentiation processes within different tissues.
AKR1C1/AKR1C2 have links to hormone-related cancers such as prostate and breast cancer. These enzymes impact the local hormone levels affecting cancer progression and response to therapy. Alterations in AKR1C1 and AKR1C2 expression or function can lead to hormone imbalances influencing cancer risk and treatment outcomes. Through their modulation of steroid hormones they connect to the activity of proteins like androgen and estrogen receptors which are critical in the pathogenesis of hormone-driven cancers.
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This species and application combination has not been tested, but we predict it will work based on strong homology. However, this combination is not covered by our product promise.
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Terms & Conditions.
0.3% PBST was used as a blocking buffer in all incubation steps. The high background signal in Mouse tissue sample was caused by the direct reaction between the Mouse IgG in Mouse tissue preps and the Goat anti-Mouse secondary antibody.
All lanes: Western blot - Anti-AKR1C1/AKR1C2 antibody [4B6AF3] (ab131375) at 2 µg/mL
Lane 1: Molecular weight marker
Lane 2: HeLa Cell Lysate at 15 µg
Lane 3: HepG2 Cell Lysate at 15 µg
Lane 4: Human Liver Homogenate (HLH) at 10 µg
Lane 5: Human Heart Homogenate (HHH) at 10 µg
Lane 6: Mouse Liver Homogenate (MLH) at 10 µg
Lane 7: Rat Liver Homogenate (RLH) at 10 µg
Lane 8: Rat Heart Homogenate (RHH) at 10 µg
All lanes: Goat anti-Mouse AP at 1/3000 dilution
Predicted band size: 37 kDa
Immunofluorescence analysis of AKR1C1 in HeLa cells, using ab131375 at 5 μg/ml.
The cells were paraformaldehyde fixed (4%, 20 minutes) and Triton X-100 permeabilized (0.1%, 15 min). The cells were then incubated with ab131375 for 2h at room temperature or over night at 4°C. The secondary antibody was (red) Alexa Fluor® 594 Goat anti-Mouse IgG (H+L) used at a 1/1000 dilution for 1h. 1% BSA was used as the blocking agent for all blocking steps. The target protein locates to the cytosol.
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